Continuous and intermittent flow

Question 1

Structure/ function of elastic arteries and how this allows for conversion of intermittent pumping to continuous flow

Answer 1

• Elastic arteries: converts intermittent pumping of heart to continuous flow through circulation, heart only ejects blood for 1/3 of cardiac cycle, tissues need blood all time
• Changes in pressure in left ventricle oscillates between 0-120mmHg
• Dampening of pressure changes by aorta and elastic arteries means blood pressure is maintained, sufficient pressure throughout each cardiac cycle ensures all tissues (particularly the brain) are perfused with blood at all times
• Structure of walls allows for dampening of pressure changes as elastin is very stretchy, it allows arteries to expand during systole (energy used to stretch the vessel is also stored as potential energy), walls contains collagen (stiffer than elastin) to protects arteries from over-distension during systole
• End of systole, when ventricle stops ejecting blood, potential energy stored in elastin is returned to blood to give it kinetic energy to carry on flowing around the circulation and so blood is being propelled at all times during cardiac cycle
• Intermittent ejection of the heart is converted to continuous flow by stretching and recoiling of elastic arteries (protein in elastin is key in this)
• Stretching and recoiling of elastic arteries impacts blood pressure, during systole, blood enters aorta stretches vessel but it is still confined within a limited space due to collagen meaning pressure ↑ to systole pressure (around 120mmHg) and during diastole blood is leaving aorta, as it recoils pressure remains high (around 80mmHg) compared to pressure in ventricles (around 5mmHg) as muscle completely relaxes dropping down to very low pressures
• Characteristics of aortic pressure wave and systolic/diastolic pressures reached
  determine mean ABP and mean ABP determines tissue perfusion

Question 2

Factors determining systolic, diastolic, mean ABP

Answer 2

• Arterial blood pressure is determined in elastic arteries, is driving force for flow
• Systolic pressure = highest pressure reached during cardiac cycle
• During systole, pressure in aorta rises rapidly as blood is ejected from aorta, stretching elastin found in tunica media, during diastole no blood is being ejected in aorta so pressure gradually falls = lowest pressure reached during cardiac cycle (occurs just before the aortic valves open)
  * Pulse pressure = systolic pressure - diastolic pressure
• Pressure wave generated in aorta is propagated along elastic arteries
• Mean ABP is not arithmetic mean of systolic and diastolic pressures
  * Mean arterial blood pressure=DP+((SP-DP))/3
• Mean ABP determine circulatory perfusion, low mean ABP = ↓ perfusion to brain
• 3 factors determine systolic/diastolic pressure and mean ABP: elastin content in artery, SV ejected into aorta, and TPR
• Systolic pressure determined by SV, aortic/arterial distensibility, ejection velocity and diastolic pressure of previous beat
• Increasing systolic pressure: ↑ EDV preload = ↑ SV → ↑ venous return, ↑ contractility (increase ejection velocity) due to ↑ in sympathetic activity to ventricular muscle or ↑ circulating adrenaline → ↑ SV, arterial system has limited capacity so systemic vascular resistance will limit how much/how fast blood escapes from aorta causing aorta and rest of arterial system to stretch and expand to accommodate full ventricular SV, and ↓compliance (due to ageing) → increase in systolic pressure
• Diastolic pressure determined by arteriolar resistance: vasoconstriction ↑ DP, increased TPR/vasodilation decrease DP, atherosclerosis ↑ DP, aortic/arterial distensibility in which reductions in distensibility (less recoil) results in decreased DP, and high heart rate ↑ DP (less time for blood to run off into periphery before next beat so starting subsequent cardiac cycle at higher DP)

Question 3

Structure and function of capillaries

Answer 3

• Capillaries = circulation’s exchange vessel, formed exclusively from endothelial cells, 1 cell thick, 2 endothelial cells form a lumen through which RBCs can move
• Neighbouring cells are a very short distance away
• Most capillaries are continuous and are found in tissues like heart, skeletal muscle, skin, and lungs, but in some tissues capillaries are fenestrated (pores), found in kidney and in exocrine glands, tissues commonly have a role of filtering fluid as fenestrations make it easier for fluid to leave capillaries
• Capillaries are involved in exchange by 2 mechanisms: diffusion and filtration (between vascular compartment and other extracellular fluid compartments)
• Blood in capillaries move at a very low velocity as they have a high total cross-sectional area and slowing blood down is good for diffusion and filtration

Question 4

Factors determining capillary filtration

Answer 4

• Starling’s forces are factors that affect fluid filtration, 4 different pressures determine movement of fluid in or out of capillaries
• Favouring filtration out of capillaries:
  1. Capillary hydrostatic pressure (pressure that fluid inside capillary exerts on walls of capillary, dependent on blood pressure): ↑ pressure = more filtration
  2. Tissue oncotic pressure (pressure exerted by free proteins outside capillary): essentially hydrostatic pressure applied to stop fluid moving to area of higher protein concentration, healthy person should have no free proteins in tissue (close to 0)
• Pressures favour reabsorption by capillaries from tissues surrounding them:
  1. Interstitial hydrostatic pressure (pressure that fluid outside capillaries exerts): close to 0 in a healthy person, should be little fluid surrounding capillaries
  2. Plasma oncotic pressure (pressure exerted by free proteins inside capillary): plasma proteins normally present in blood tend to help to keep fluid inside capillaries
• Net filtration/overall movement of fluid is dependent on how leaky capillaries are, represented by reflection coefficient (Kf):
  * Net filtration=Kf x (forces favour filtration)-(forces favouring reabsoption)
  * Net filtration=Kf x (P_c+π_i )-(P_i+π_p)
• Blood enters peripheral capillaries with hydrostatic pressure (35mmHg), resistance → blood leaves at 15mmHg (drop creates hydrostatic pressure gradient)
• Plasma oncotic pressure = main force opposing fluid filtration, in peripheral capillaries it creates a pressure of 25mmHg (will not significantly change along length)
• Normally interstitial hydrostatic pressure and interstitial oncotic pressure is very low (0 to -3 mmHg) but in tissues surrounded by skin/bone/other physical boundaries this value can increase due to the limited expansion (impact on driving fluid to capillaries)
• Small amount protein in interstitial fluid favours movement out (negligible in health)
• Arteriole end of the capillary = net filtration of 10mmHg, end it favours filtration of fluid out but venous end = net filtration rate of -10mmHg, favours reabsorption of fluid
• Over entire length: no net movement of fluid, however if balance of pressures changes there could be net filtration out of capillary into tissues
• Additional fluid taken up by lymph vessels is drained back into blood, but increase in filtration too big for lymph system = oedema forms (build-up of fluid in body which causes affected tissues to become swollen)

Question 5

What is the impact of changes in pre-capillary resistance?

Answer 5

• Resistance in terminal arterioles, determined by arteriolar diameter, influences blood pressure reaching capillaries and directly influences capillary hydrostatic pressure
• Normal circumstances: filtration at arterial end is balanced by reabsorption at venous end but if terminal end supplying a capillary bed is constricted, radius of arteriole will be smaller so resistance will be higher
• Pressure, energy to push blood through vessel, used to overcome greater resistance in constricted arteriole, so blood capillary, when reached, is lower so capillary hydrostatic pressure will be lower too and pressure at venular end is lower
• So, lower force favouring filtration at arteriole end and greater force favouring reabsorption at venule end = net reabsorption of fluid from interstitial space
• Constricting arterioles → increase in TPR causing ↑ in ABP upstream of change in resistance but as blood has to travel through higher resistance more energy is used up, so when blood reaches capillaries, hydrostatic pressure is lower (constriction of terminal arterioles protects capillaries from higher arterial pressures)
• Effect of pre-capillary vasodilation on net filtration: if terminal arteriole supplying capillary bed is dilated, radius ↑ and resistance will be lower, pressure will not be used up as much so blood pressure ↑ when reaching capillaries, capillary hydrostatic pressure will be higher, and pressure at the venular end is higher
• Results in force favouring filtration out at arteriole end > force favouring reabsorption at venule end (net filtration of fluid into interstitial space – needs draining by lymph)
• Arteriolar vasodilation → decreased TPR so fall in mean ABP upstream from change in resistance in arterioles, blood travels through lower resistance less energy is taken up so blood reaches capillaries at higher pressure, capillary hydrostatic pressure closer to arterial blood pressure
• lymphatic vessels are thin walled, contain one-way valves to prevent backflow of fluid and return filtered fluid back into blood via subclavian veins